Gene interactions and pathways from curated databases and text-mining

◀ Back to PIK3CA

NGF — PIK3CA

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Ye et al., Cell 2000 : Thus, PIKE physiologically modulates the activation by NGF of nuclear PI3K
Ye et al., Nature 2002 : PIKE is a nuclear GTPase that activates nuclear PI(3)K activity, and mediates the physiological activation by nerve growth factor (NGF) of nuclear PI(3)K activity
Nusser et al., J Biol Chem 2002 : Taken together, these data indicate that NGF mediated activation of TrkA receptor stimulates PI3K , which in turn increases Rac1 activity to induce transient RhoA inactivation during the initial phase of neurite outgrowth
Halvorsen et al., Brain Res 2002 (MAP Kinase Signaling System...) : Survival promoting MEK-ERK and PI3K pathways contribute to viability during MPP ( + ) exposure, both are activated by NGF , and loss of PI3K mediated signaling and NF-kappa B-mediated transcription may commit cells irreversibly to apoptosis in this model
Salinas et al., J Biol Chem 2003 : Inhibition of PI3K prevented NGF induction of HO-1 mRNA and protein and partially reversed its protective effect against 6-OHDA induced ROS release
Zhuang et al., J Neurosci 2004 (Hyperalgesia...) : ERK activation by capsaicin and NGF was also blocked by PI3K inhibitors
Ahn et al., EMBO J 2004 : Here we show that nuclear PI3K and its upstream regulator PIKE mediate the antiapoptotic activity of nerve growth factor (NGF) in the isolated nuclei
Park et al., J Biol Chem 2007 : Specifically, NGF enhanced TrkA phosphorylation, PI3K activity, and Akt phosphorylation
Tucker et al., Cell Signal 2008 : Inhibition of either Src or FAK activity attenuated both laminin and/or NGF induced PI 3-K/Akt and MEK/MAPK signalling pathways, as well as neurite growth
Kim et al., Neurochem Int 2010 : Additionally, NPPB and SITS, another chloride channel blocker, suppressed NGF induced TrkA phosphorylation and subsequent PI3K/Akt phosphorylation and Rac1 activation in PC12 cells
Niewiadomska et al., Behav Brain Res 2011 (Alzheimer Disease) : NGF released from target cells activates TrkA on axon terminals and triggers activation of PI3K/Akt , MEK/ERK, and PLC? ( phospholipase C ) signaling pathways
Ketschek et al., Communicative & integrative biology 2011 : Thus, NGF increases formation of axonal filopodia through localized PI3K signaling that promotes the initiation of actin patch precursors to the formation of axonal filopodia
Liu et al., Exp Mol Med 2013 : Similar to the changes in neurite outgrowth, the PI3K/Akt activation by NGF was potentiated by PIP5Ka KD, but was attenuated by the reintroduction of PIP5Ka